Anti arrhythmic agents Flashcards
Arrhythmia
Arrhythmias are defined as:
1) changes in rhythm source localization;
2) changes in heart rate;
3) irregular rhythm;
4) electrical impulse spreading (conduction) disturbances
Classification of arrhythmias
- Rhythms and arrhythmias of the sinus node
- Supraventricular arrhythmias
- Atrial arrhythmias independent of AV node
- AV node dependent arrhythmias - Ventricular arrhythmias
- Disorders of intratrial and interatrial conduction
- Atrioventricular conduction disorders
- Intraventricular conduction disorders
Singh Vaughan Williams classification of antiarrhythmic drugs
A) Class Ia inhibits ** Na + flux *** CM in phase 0
and inhibits K + flow in CM phase 3
B) Class Ib inhibits the Na + flux in CM phase 0 and
accelerates K + flow in CM phase 3
C) Class Ic inhibits the Na + flux in CM phase 0
D) Class II inhibits Ca2 + flux in SA and AV phases 0
and 4
E) Class III inhibits K + flux in CM phase 3
F) Class IV inhibits Ca2 + flux in SA and AV phases 0
and 4
Class 1 A
Procainamide
1. Na + channel blocker with medium dissociation kinetics
Delays the Na + flux in CM phase 0 by expanding the QRS complex
2. K+ channel blocker, inhibits K + cardiomyocytes in Phase 3 DP
(prolongs repolarization) by prolonging the QT interval
It also has a cholinolytic effect
Treatment of supraventricular arrhythmias (SVA)
Ventricular arrhythmia (VA) treatment
SE: hypotension, lupus erythematodes syndrome, *TdP
Class IA has a pronounced proarrhythmic effect -
the ability of the drug to aggravate or provoke an existing arrhythmia
new arrhythmias not previously detected
Class 1 B
Lidocaine 1. Na + channel blocker with fast dissociation kinetics Delays the Na + flow in CM phase 0, but the QRS complex remains unchanged, because the class is characterized by fast DK 2. K+ channel activation cardiomyocytes in DP phase 3 (shortens repolarization) The QT interval is reduced or unchanged
VA treatment
SE: CNS toxicity (cramps)
Lidocaine - presystemic inactivation (do not use p / o)!
Class 1 C
IC klase Propafenon
Flecainid
1. Na + channel blockers with slow dissociation kinetics
Delays the Na + flux in KM phase 0 by expanding the QRS complex
- K + channels and repolarization are not affected
SVA (including control of the Afib rhythm)
SE: heart failure
Amiodarone
CLASS IA, 2,3,4
1. K + channel blocker, inhibits K + flux in CM phase 3 (prolongs repolarization), prolongs QT interval. Matches class III mechanism of action 2. Na + channel blocker, inhibits Na + flux in CM phase 0, expands QRS complex. Matches class Ia mechanism of action 3. Beta blocker, inhibits Ca2 + flux in SA phases 0 and 4, prolongs RR interval - «-» chronotropy, inhibits Ca2 + flux in AV phases 0 and 4, prolongs PR interval - «-» dromotropy, as well as inhibiting Ca2 + flux in CM phase 2 - «-» inotropy. Matches class II mechanism 4. Calcium channel blocker, inhibits Ca2 + flux in SA phases 0 and 4, prolongs RR interval - «-» chronotropy, inhibits Ca2 + flux in AV phases 0 and 4, prolongs PR interval - «-» dromotropy, and inhibits Ca2 + flow CM in phase 2 - «-» inotropy. Corresponds to the class IV mechanism of action
SVA (also Afib)
VA treatment
SE: hypothyroidism, hyperthyroidism pneumofibrosis, phototoxicity,
hepatotoxicity,
bluish skin pigmentation (smurf skin), corneal deposition, rarely TdP
Vernakalant
CLASS 1 B, 3
1. K + channel blocker, inhibits K + flow in CM phase 3 (prolongs repolarization), prolongs the QT interval. Matches class III mechanism of action 2. Na + channel blocker with fast dissociation kinetics Delays the Na + flow in CM phase 0, but the QRS complex remains unchanged, because the class is characterized by fast DK Matches class IB mechanism of action Selective extension of atrial AP because of inhibition of K + flow, which is specific to the anterior chamber only. The specific K + flow is determined by the K + channel type.
Acute Afib treatment
SE: hypotension, bradycardia
CLASS 2
BAB
Reduces the effects of SNS (stress) on cardiac conduction system and automaticity
Propranolol
Metoprolol
Bisoprolol
Beta1 adrenoceptor blockade in the SA node and especially in the AV node
Delays Ca2 + flux in SA phases 0 and 4, prolongs RR interval - «-» chronotropy,
inhibits Ca2 + flux in AV phases 0 and 4, prolongs PR interval - «-» dromotropy,
as well as inhibiting Ca2 + flux in CM phase 2 - «-» inotropy.
Frequency control of SVA (eg, Afib, sinustachycardia)
VA treatment
CLASS 4
Ca2+ channel blockers
Verapamil
Diltiazem
Ca2+ channel blockade
Delays Ca2 + flux in SA phases 0 and 4, prolongs RR interval - «-» chronotropy,
inhibits Ca2 + flux in AV phases 0 and 4, prolongs PR interval - «-» dromotropy,
as well as inhibiting Ca2 + flux in CM phase 2 - «-» inotropy.
Frequency control of SVA (eg, Afib, sinus tachycardia)
Magnesium sulfate
Reduces Ca2+ flow in ventricular cardiomyocyte
TdP treatment
Atropine
«+» chrono-, «+» dromotropic effect
Sinus bradycardia
AV node block
Epinephrine
«+» ino-, «+» chrono-, «+» dromotropic effect
CPR
Digoxin
”-“ chronotropic and “-“ dromotropic effects
(suppresses AV transmission)
SVA Rhythm Disorders (Afib)
However, it is not effective enough in the case of increased SNS activity,
such as during exercise. Can be used in complementary therapy with BAB or CCB
Digoxin overdose
For the prophylaxis potassium mediactions potassium, magnesium aspartate
In case of severe toxicity - ventricular tachycardia -
phenytoin prescribing is required
and antibodies (digoxin immune Fab) that inactivate the drug
Prolonged QT syndrome
Mainly caused by mainly by inhibiting the flow of Ikr (hERG)
hERG - one of the K + channels responsible for repolarization
Of all the antiarrhythmic agents, class IA and III drugs are most at risk. QT interval may also be extended by medications from other classes of drugs, such as histamine receptor antagonists, antibiotics
